EC Number   |
Natural Substrates |
|---|
    1.6.1.2 | more |
diabetes is potentially linked to a defective transhydrogenase gene |
| 1.6.1.2 | more |
the glucose intolerance and impaired insulin secretion of the C57BL/6J mouse strain results from oxidative stress due to a mutated nicotinamide nucleotide transhydrogenase. Mutation of this gene in a mouse strain with normal insulin secretion results in strong glucose intolerance |
| 1.6.1.2 | more |
insulin hypersecretion is associated with increased Nnt expression. It can be suggest that nicotinamide nucleotide transhydrogenase must play an important role in beta cell function |
| 1.6.1.2 | more |
with ongoing NADPH and NAD+ generation, the proton-translocating, mitochondrial transhydrogenase can serve as an additional anaerobic phosphorylation site |
| 1.6.1.2 | NADH + NADP+ |
links hydride transfer between NAD(H) and NADP(H) to the outside-in translocation of protons across membrane |
| 1.6.1.2 | NADH + NADP+ |
links hydride transfer between NAD(H) and NADP(H) to the translocation of protons across membrane |
| 1.6.1.2 | NADH + NADP+ |
links hydride transfer between NAD(H) and NADP(H) to the translocation of protons across membrane, hydride ion equivalent is transferred from the A side of NC4 of NADH to the B side of NC4 of NADP+, provides NADPH for metabolic biosynthesis and reduction of glutathione |
| 1.6.1.2 | NADH + NADP+ |
links hydride transfer between NAD(H) and NADP(H) to the translocation of protons across membrane, important as source of NADPH for biosynthesis and glutathione reduction |
| 1.6.1.2 | NADH + NADP+ |
links hydride transfer between NAD(H) and NADP(H) to the translocation of protons across membrane, important for the oxidative stress defense |
| 1.6.1.2 | NADH + NADP+ |
links hydride transfer between NAD(H) and NADP(H) to the translocation of protons across membrane, major source of NADPH, provides reducing agent for glutathione and is therefore important for the oxidative stress defense |
